Objective To evaluate the effect of procedure for prolapse and hemorrhoid(PPH)for the treatment of prolapsed internal hemorrhoids. Methods 23 patients with the third or fourth degree circular prolapsed internal hemorrhoids were managed by means of PPH. Results The mean operative time was 22 minutes,and hospital stay was 3.5 days after operation.Pain in 48 hours after operation was evaluated and 18 cases had no pain(78 3%),5 cases less pain(21 7%).The anastomoses healed in (4～5) weeks and there was no recurrence in (1～6) months after the patients were discharged from hospital. Conslusions Compared with the traditional operation,PPH has the advantages of simpleness,less pain,less complications and quiker recovery,but the cost is higher.

Objective:To investigate the chemical constituents from Avicennia marina.Methods:The isolation and purification of the CH2Cl2 and n-BuOH fractions of this plant were performed,and the chemical structures were elucidated by spectral analysis as well as comparison of their spectral data with literature values.Results:Three novel compounds were obtained and identified as erythro-guaiacylglycerol-?-ferulic acid ether(1),marinnone A(16) and marinnone B(17),along with eighteen known compounds as threo-guaiacylglycerol-?-ferulic acid ether(2),eleutheroside E2(3),(+)-lirioresinol A(4),dihydroxymethyl-bis(3,5-dimethoxy-4-hydroxyphenyl) tetrahydrofuran-9-O-?-glucopyranoside(5),(+)-lyoniresinol 3a-O-?-D-glucopyranoside(6),(-)-lyoniresinol 3a-O-?-D-glucopyranoside(7),epi-pinoresinol(8),leucoseceptoside A(9),jionoside C(10),salsaside A(11),ilicifolioside A(12),acteoside(13),isoacteoside(14),ethyl ferulate(15),avicennone D(18),avicenone E(19),avicennol C(20),and stenocarpoquinone B(21).Conclusion:Three new compounds(1,16 and 17) were obtained and thirteen known compounds,2-12,14 and 15 were isolated from Avicennia genus for the first time.

Objective To investigate the variation of corticotropin-releasing hormone(CRH)in plasma,the mRNA and protein expression of c-Fos and gap junction gene connexin-43(Cx43)in the myometrium of term pregnancy women,and to study the correlations among CRH,Cx43 and c-Fos at onset of labor.Methods 30 cases in labor(L group),30 cases not in labor(NL group)but in term pregnancy, and 30 cases of non-pregnant(NP group)women undergoing hysterectomy due to cervical intraepithelial neoplasia were recruited into this clinical study.Radioimmunoassay was employed to measure the concentration of CRH in plasma;in situ hybridization assay and streptravidin-biotin peroxidase(SP) immunohistoehemical techniques were respectively used to detect the expression levels of c-Fos mRNA,Cx43 mRNA and the corresponding proteins.Results(1)The concentration of CRH in L group(81.8?11.9) pmol/L was significantly higher than that in NL group(34.5?18.6)pmol/L(P

Objective:To study the expression of Survivin,VEGF,p53 and their correlation inbreast cancer, 22 cases of hyperplasia of mammary gland and 10 cases of paracainoma normal tissues by immunohistochemical technique (SP).Results: The positive rates of Survivin were 76.7%,18.2% and 0% in breast cancer, hyperplasia of mammary gland and paracacinoma normal tissues (P

Objective By detecting the variation of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) DNA methylation in preeclampsia-like mouse models generated by different ways, to explore the roles of multifactor and multiple pathways in preeclampsia pathogenesis on molecular basis. Methods Established preeclampsia-like mouse models in different ways and divided into groups as follows: (1) Nw-nitro-L-arginine-methyl ester (L-NAME) group: wild-type pregnant mouse received subcutaneous injection of L-NAME;(2) lipopolysaccharide (LPS) group:wild-type pregnant mouse received intraperitoneal injection of LPS; (3) apolipoprotein C-Ⅲ (ApoC3) group: ApoC3 transgenic pregnant mouse with dysregulated lipid metabolism received subcutaneous injection of L-NAME;(4)β2 glycoprotein I (β-2GPI) group:wild-type pregnant mouse received subcutaneous injection ofβ-2GPI. According to the first injection time (on day 3, 11, 16 respectively), the L-NAME, LPS and ApoC3 groups were further subdivided into:pre-implantation (PI) experimental stage, early gestation (EG) experimental stage, and late gestation (LG) experimental stage.β-2GPI group was only injected before implantation. LCHAD gene methylation levels in placental were detected in different experimental stage. Normal saline control groups were set within wild-type and ApoC3 transgenic pregnant mice simultaneously. Results (1) CG sites in LCHAD DNA:45 CG sites were detected in the range of 728 bp before LCHAD gene transcription start site, the 5, 12, 13, 14, 15, 16, 19, 24, 25, 27, 28, 29, 30, 31, 32, 34, 35, 43 CG sites were complex sites which contained two or more CG sequences, others were single site which contained one CG sequence. The 3, 5, 6, 11, 13, 14, 18, 28 sites in L-NAME, LPS, ApoC3 and β-2GPI groups showed different high levels of methylation; the 16, 25, 31, 42, 44 sites showed different low levels of methylation; other 32 sites were unmethylated. (2) Comparison of LCHAD gene methylation between different groups:the methylation levels of LCAHD gene at 3, 11, 13, 14, 18 sites in L-NAME, LPS, ApoC3 andβ-2GPI groups were significantly higher than those in the normal saline control group (P<0.05); and the methylation levels of 42, 44 sites in these groups were significantly lower than those in the normal saline control group (P<0.05). (3) Methylation of LCHAD gene at the same site between different experimental stages: ① The 3, 11, 18 sites of EG experimental stage was significantly lower than PI and LG experimental stage in L-NAME group (P<0.05);the 3, 11, 18 sites of PI experimental stage was significantly lower than EG and LG experimental stage in LPS group (P<0.05);these sites of PI experimental stage was significantly higher than EG and LG experimental stages in ApoC3 group (P<0.05).②The methylation of site 5 in L-NAME and LPS groups were significantly higher than that of the normal saline control group (P<0.05), and the LG experimental stages were significantly higher than other stages, but in ApoC3 group , only PI and EG stages were significantly higher than the normal saline control group (P<0.05).③At site 6 in L-NAME group which showed high methylation level was significantly higher than the same site in other groups which showed low methylation level (P<0.05).④At 13, 14 sites, earlier preeclampsia onset caused a lower methylation level in L-NAME group, but PI experimental stage was significantly higher than EG and LG experimental stages in LPS group (P<0.05), EG experimental stage was significantly higher than PI and LG experimental stages in ApoC3 group (P<0.05). ⑤ At site 28, earlier preeclampsia onset caused a higher methylation level in L-NAME group, but PI experimental stage was significantly lower than EG and LG experimental stages in LPS group (P<0.05), EG experimental stage was significantly higher than PI and LG experimental stages in ApoC3 group (P<0.05).⑥The 16, 25, 31 sites in ApoC3 group were significantly higher than other groups (P<0.05). ⑦ At site 42 in β-2GPI group was unmethylated, but it in other groups showed low methylation level, the methylation level of site 42 inβ-2GPI group was significantly lower than that in other groups (P<0.05). Conclusions The methylation of 6 and 42 CG sites may be related to LCHAD gene expression in placenta of L-NAME and β-2GPI induced preeclampsia-like models respectively;LCHAD gene expression and DNA methylation may not have obviouscorrelation in LPS and ApoC3 induced preeclampsia-like models. Differences exist in LCHAD DNA methylation in preeclampsia-like models generated by different ways, revealed a molecular basis to expand our understanding of the multi-factorial pathogenesis of preeclampsia.

Objective To investigate the influence of obesity on renal lesion in IgA nephropathy (IgAN) patients by analyzing the association between obesity and absolute renal risk factors (ARR).Method Clinical-pathological data of IgAN patients diagnosed by renal biopsy in General Hospital of Ningxia Medical University were collected retrospectively.According to the body mass index (BMI),patients were divided into non-obese group (BMI ＜ 28,N-OB group) and obese group (BMI≥28,OB group).Their clinical characteristics,pathological index and ARR scores were compared.The relationship of BMI and ARR was analyzed by ordinal logistic regression models.Results (1) A total of 674 IgAN patients with mean age of 35.5+ 11.3 years were enrolled,including 94 in OB group and 580 in N-OB group respectively.Compared with those in the N-OB group,the proportion of male,age,mean arterial pressure,blood uric acid,blood triglyceride,diabetes mellitus and hypertension increased in OB group (all P ＜ 0.01).Patients in OB group had lower estimated glomerular filtration rate (eGFR) and higher ARR score than those in N-OB group (all P ＜ 0.05).(2) More severe thickening renal small artery wall and hyaline degeneration were observed in the OB group than in the N-OB group (all P ＜ 0.01).There was no statistical difference between the two groups in Lee classification,Oxford classification,mesangial cell proliferation,glomerular sclerosis,crescent formation,renal tubular atrophy,interstitial inflammatory cell in filtration and endothelial cell proliferation.(3) After adjusting for age,sex,blood uric acid,serum albumin,eGFR,low density lipoprotein,glomerular sclerosis,interstitial inflammatory cell infiltration,renal tubular atrophy and vascular wall thickening,BMI was still an independent risk factors for ARR in IgAN patients (OR=1.09,95％ CI 1.03-1.14).Conclusions BMI is an independent risk factors for ARR in IgAN patients.Early prevention and control of obesity and its associated risk factors may improve outcomes of IgAN patients.

Objective To investigate the effect of autophagy on the proliferation and migration of cervi-cal cancer cells ,as well as the underlining mechanisms .Methods Rapamycin was used to induce the autophagy in HeLa cells,formation of autophagosomes was observed by staining with acridine orange under fluorescence mi -croscope.Western blot was used to detect the expression of LC 3 and PI3K/Akt/mTOR in HeLa cells.The LC3 plasmid was transfected into HeLa cells .The distribution of LC3 in cells and the expression of LC3 was identified by fluorescence microscope and Western blot ,respectively.The autophagy was inhibited with 3-methyladenine(3-MA )in HeLa cells.The cell proliferation was monitored by RTCA real -time instrument.Transwell chamber was carried out to assess cell migration .Results After 6h of rapamycin treatment ,the expression of LC3B was in-creased in HeLa cells ( P<0 .05 ) .The proliferative and migration ability were weakened compared to wild type HeLa cells(P<0.05).The same results in the presence of 3-MA.The expression of PI3K/AKT/mTOR path-way proteins were activated by rapamycin treatment and LC 3 overexpression(P<0.05).Conclusion Autophagy can suppress the proliferation and migration in cervical cancer cells ,which may relate to PI3K/Akt/mTOR path-way.

Tumor cell plasticity, including epithelial to mesenchymal transition (EMT) and its reverse program, mesenchymal to epithe-lial transition (MET), regulates circulating tumor cells and carcinoma metastasis. Twist is overexpressed in rhabdomyosarcoma, breast cancer, gastric cancer, and other tumors. Twist, as a transcriptional factor, cross-talks with multiple signaling pathways, forming a com-plex network to participate in the regulation of EMT/MET in circulating tumor cells, which in turn promotes metastasis of tumor cells. Therefore, monitoring the level of Twist and epithelial–mesenchymal phenotypic molecules is important as it may be beneficial for in-creasing the detection ratio of circulating tumor cells as tumor biomarkers and for evaluating the effects of anticancer drugs.

Pregnancy ; Humans ; Female ; Cesarean Section/adverse effects* ; Abdominal Cavity ; Neoplasms

Objective To investigate the mechanism of BVT. 2733 on insulin resistance, by using diet-induced obese (DIO) mice model. Methods After having been balanced for 3 days, the C57BL/6J mice were randomly divided into a normal diet group and a high-fat diet (HFD) group. After 20 weeks, the obese mice were further randomly divided into an obese control group, a BVT. 2733 group and a pioglltazone (PGZ) group and they were orally administered with placebo, BVT. 2733 and PGZ separately for two weeks.Adiponectin and leptin mRNA expression levels from adipose tissue were analyzed with real-time quantitative PCR. The levels of plasma glucose, serum insulin and adiponectin were measured with biochemical technology, radioimmunoassay and ELISA. Adipocyte sizes were observed with immunohistocbemistry.Results The body weight, plasma glucose and serum insulin levels raised(P<0.05)in the HFD group and the adipocyte sizes were bigger. Serum insulin levels significantly reduced (P<0.05) and adipocyte sizes reduced, while plasma adiponectin level raised (P<0.01)in the two treatment groups as compared with those in obese controls. Both the mRNA expressions of adiponectin and leptin upregulated(P<0.05)in the PGZ group, but their expressions in the BVT. 2733 group did not alter significantly. The body weight of the mice reduced significantly in the BVT. 2733 group. Conclusion BVT. 2733 can reduce body weight significantly and improve insulin resistance, but cannot influence the expression of adipocytokines.